Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indirect immunofluorescence staining revealed that endometrial stromal cells (ESC) in the ectopic endometrium of patients with endometriosis or adenomyosis expressed aminopeptidase N/cluster of differentiation (CD) 13 antigen and neutral endopeptidase/CD10 antigen, both of which are expressed on ESC in the normal endometrium throughout the menstrual cycle. Thus, ESC in the ectopic endometrium resembled ESC in the normal endometrium not only morphologically but also antigenically. Both peptidase antigens may be useful markers for the histological diagnosis of endometriosis and adenomyosis.
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PMID:Expression of aminopeptidase N and neutral endopeptidase on the endometrial stromal cells in endometriosis and adenomyosis. 136 4

Using the immunohistochemical technique, we investigated the expression of CD10 in normal female genital tissues, chorionic villi and decidua of early gestation, endometriotic lesions, and uterine mesenchymal tumors. The cytoplasm of normal endometrial stromal cells was consistently positive for CD10. During early gestation, decidualized endometrial stromal cells were negative or only focally positive for CD10, whereas nondecidualized stromal cells were diffusely positive. Syncytiotrophoblast was positive for CD10 on the apical surface, whereas chorionic mesenchymal cells were diffusely positive within the cytoplasm. Cytotrophoblast and intermediate trophoblast were negative for CD10. Groups of stromal cells surrounding cervical glands were often positive for CD10. Myometrium, endometrial and cervical glands, cervical squamous epithelia, and tubal epithelia and stroma exhibited no reactivity for CD10. In endometriosis and adenomyosis, ectopic endometrial stromal cells were usually positive for CD10. Endometrial stromal tumors, including undifferentiated uterine sarcomas, mostly showed diffuse immunoreactivity for CD10. Leiomyomas and leiomyosarcomas were negative or focally (< 5% of cells staining) positive (8/12 leiomyomas and 4/8 leiomyosarcomas) for CD10, except for 1 myxoid leiomyosarcoma that showed CD10 staining in the myxoid areas. These data suggest that diffuse CD10 staining is characteristic of normal and neoplastic endometrial stromal cells, unless they are decidualized.
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PMID:CD10 is a marker for normal and neoplastic endometrial stromal cells. 1178 22

Adenomyosis may be involved by endometrial adenocarcinoma, but in contrast to true myometrial invasion, the depth of an adenomyotic focus involved by carcinoma does not alter pathologic tumor staging. Therefore, distinction from carcinoma invading myometrium is clinically relevant. We hypothesized that CD10, a marker of non-neoplastic and neoplastic endometrial stroma, would highlight the stromal component of adenomyotic foci and be useful in this distinction. Thirty-nine cases of endometrial adenocarcinoma were analyzed and divided into three groups: I, invasive endometrial adenocarcinoma (n = 14); II, endometrial adenocarcinoma involving adenomyosis but without myometrial invasion (n = 18); and III, adenomyosis involved by endometrial adenocarcinoma with concomitant invasive component (n = 7). All cases of adenomyosis involved by endometrial adenocarcinoma demonstrated CD10 expression in the stromal cells of adenomyotic foci. Eleven of 21 cases (52%) of invasive adenocarcinoma also showed CD10 expression, at least focally, in cells immediately surrounding the infiltrating glands. Of these, two cases (from Group III) also had associated adenomyotic involvement by carcinoma. The remaining cases of invasive carcinoma were negative for CD10. Therefore, presence of CD10 staining immediately surrounding neoplastic glands does not equate with involvement of adenomyosis by endometrial adenocarcinoma. In contrast, absence of CD10 expression excludes involvement of adenomyosis by adenocarcinoma.
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PMID:The role of CD10 staining in distinguishing invasive endometrial adenocarcinoma from adenocarcinoma involving adenomyosis. 1252 9

The distinction of involvement of adenomyosis by endometrial carcinoma from endometrial carcinoma invading the myometrium can at times be difficult. This distinction, however, is important from the standpoint of staging, treatment, and prognosis because the outcome of carcinoma invading the myometrium as compared with involving adenomyosis is significantly worse. CD10 has been recently reported to be expressed by normal and neoplastic endometrial stromal cells. We therefore hypothesized that CD10 may be helpful in distinguishing carcinoma within adenomyosis from endometrial carcinoma directly invading the myometrium. Twenty-two cases of invasive endometrioid adenocarcinoma were identified from the surgical pathology files of the Johns Hopkins Hospital and consultation files of one of the authors (R.J.K.) and immunostained for CD10, desmin, and caldesmon. The pattern of staining was compared with five cases in which carcinoma was confined to adenomyosis. As a control, 14 cases of adenomyosis unassociated with carcinoma were included in the analysis. All 22 endometrial carcinomas that invaded the myometrium expressed CD10 to some extent in cells immediately surrounding the neoplastic glands. In 18, all of the invasive nests displayed CD10 in surrounding cells, but in four cases the staining was patchier, involving the surrounding cells of approximately 50-75% of the invasive nests. In four cases of myoinvasive carcinoma, the CD10-positive cells surrounding the nests of invasive carcinoma were also positive for desmin and caldesmon. In the remaining 18 cases with myoinvasive carcinoma, the cells surrounding the carcinomas failed to react with desmin and caldesmon. All five endometrial carcinomas involving adenomyosis displayed CD10 positivity in what appeared to be endometrial stromal cells surrounding the neoplastic glands. The stromal cells were negative for desmin and caldesmon. The control cases of adenomyosis were all positive for CD10, although in four cases the staining was patchy compared with 10 cases in which it was diffuse. Desmin and caldesmon were negative in all of these cases. Although CD10 identifies endometrial stromal cells in the endometrium and in adenomyosis and endometriosis, this study demonstrates that CD10 does not aid in distinguishing myometrial invasion of endometrial carcinoma from involvement of adenomyosis by endometrial carcinoma because the cells surrounding the tumor in the myoinvasive group express CD10.
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PMID:CD10 imunostaining does not distinguish endometrial carcinoma invading myometrium from carcinoma involving adenomyosis. 1276 82

The present study aimed to investigate oxytocin receptor (OTR) expression in the normal uterus, and particularly in uterine smooth muscle tumors and endometrial stromal sarcomas (ESSs) because these tumors can be difficult to distinguish. The expressions of OTR, CD10, h-caldesmon, calponin, smooth muscle actin, and desmin were analyzed in 10 conventional leiomyomas (LMs), 10 highly cellular leiomyomas (HCLs), eight leiomyosarcomas (LMSs), and nine ESSs. In five normal uteri and five cases of adenomyosis, OTR was strongly expressed in the myometrium and showed expression pronounced in the surface epithelium during the late proliferative phase and at the time of ovulation, whereas the endometrial stromal cells were negative. All LMs and HCLs were strongly positive for OTR. Five cases of LMS showed moderate to strong OTR expression in 100% of the tumor cells, whereas three cases were weakly positive in 10-20% of the tumor cells. Every ESS was negative for OTR, except in regions of smooth muscle differentiation. All ESSs were positive for CD10, as were one LM, six HCLs, and five LMSs. The ESSs were negative for h-caldesmon and showed desmin positivity mainly in regions of smooth muscle metaplasia. h-Caldesmon, calponin, smooth muscle actin, and desmin were expressed in all LMs, HCLs, and LMSs except for one leiomyosarcoma with epithelioid features, which was negative for h-caldesmon and calponin. Our study indicates that the evaluation of OTR expression is useful in the distinction of uterine smooth muscle tumors from ESSs, and that the OTR is expressed in normal and neoplastic uterine smooth muscle cells.
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PMID:Use of oxytocin receptor expression in distinguishing between uterine smooth muscle tumors and endometrial stromal sarcoma. 1457 80

A case of nodular histiocytic hyperplasia of the endometrium is described. A 45-year-old Japanese woman was found to have an enlarged uterus during her annual checkup. Hysterectomy and bilateral salpingo-oophorectomy specimens revealed uterine leiomyomas, adenomyosis, and acute salpingitis. A 5-mm, well-demarcated, elevated endometrial nodule (an incidental finding) was present and consisted of round or polygonal histiocytic cells with eccentric nuclei and pale or granular cytoplasm. The nuclei were ovoid, reniform, or crescent-shaped and had fine chromatin and inconspicuous nucleoli, and the cytoplasm contained single or multiple vacuoles. Immunohistochemically, the histiocytic cells were positive for vimentin, CD68, and lysozyme and were negative for cytokeratin, S100 protein, estrogen and progesterone receptors, and CD10. Nodular histiocytic hyperplasia in the endometrium is considered to be a reactive process. Differentiation from neoplasms, including signet-ring cell carcinoma, in curettage specimens is critical to avoid unnecessary surgical resection.
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PMID:Nodular histiocytic hyperplasia of the endometrium. 1533 51

Adenomyosis is commonly seen in hysterectomy specimens for endometrial adenocarcinoma where it could be involved with the tumor. When adenocarcinoma involves adenomyosis, the tumor may remain limited to the adenomyosis or proceeds to invade the adjacent myometrium. The purpose of this study was to investigate whether the risk of myometrial invasion by grade 1 endometrioid adenocarcinoma in cases with cancer-positive adenomyosis is different from that of cases where cancer occurs in the absence of adenomyosis. Forty-six consecutive hysterectomy specimens with International Federation of Gynecology and Obstetrics (FIGO) grade 1 endometrial endometrioid adenocarcinoma involving adenomyosis and 49 consecutive specimens with the same tumor occurring in the absence of adenomyosis were retrospectively studied by 4 experienced gynecologic pathologists. In cases with adenomyosis, myometrial invasion was confirmed by CD10-negative staining around glands with irregular outline surrounded by inflamed desmoplastic stroma. Myometrial invasion was found in significantly more adenomyosis cases (n = 42, 91.3%) than in cases without adenomyosis (n = 38, 77.5%) (chi = 4.79, P = 0.03). In 16 cases of the former group, the invasion only occurred from the foci of adenomyosis. Although myometrial invasion in the outer half was more common in the adenomyosis group (n = 16, 34.8%) than in cases without adenomyosis (n = 9, 18.4%), the difference was not statistically significant (chi = 3.29, P = 0.07). By involving coexistent adenomyosis, FIGO grade 1 endometrial endometrioid adenocarcinoma is associated with myometrial invasion, probably through increasing the surface area of its interface with the adjacent myometrium. When compared with their counterparts that occur in the absence of adenomyosis, these tumors are significantly more likely to invade the myometrium.
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PMID:Adenomyosis is associated with myometrial invasion by FIGO 1 endometrial adenocarcinoma. 1758 12

Adenomyosis is commonly seen in association with endometrial adenocarcinoma where it may or may not be involved by malignancy. This study of grade 1 endometrioid adenocarcinoma investigates whether patients with cancer-positive adenomyosis are at a different risk for deep myometrial invasion compared with those with cancer-negative adenomyosis. Ninety-three hysterectomy specimens with FIGO (International Federation of Gynecologists and Obstetricians) grade 1 endometrial endometrioid adenocarcinoma associated with adenomyosis were studied. Four experienced gynecologic pathologists retrospectively reviewed all hematoxylin and eosin-stained sections. Myometrial invasion was confirmed by CD10-negative staining around glands with jagged outline surrounded by inflamed desmoplastic stroma. Adenomyosis was involved by adenocarcinoma in 46 cases, whereas it was carcinoma-negative in 47 cases. Myometrial invasion was found in significantly more carcinoma-positive adenomyosis cases (n = 42, 91.3%) than with carcinoma-negative adenomyosis cases (n = 30, 63.8%) (chi(2) = 12.10; P = .0005). Moreover, myometrial invasion in the outer half was also seen in significantly more carcinoma-positive adenomyosis cases (n = 16, 34.8%) than with carcinoma-negative adenomyosis cases (n = 3, 6.4%) (chi(2) = 11.53; P = .0007). Among all cases of FIGO grade 1 endometrial endometrioid adenocarcinoma associated with adenomyosis, the ones that extend in the adenomyosis gain more invasive advantage, probably through increasing the surface area of its interface with the adjacent myometrium. When compared with tumors that do not involve adenomyosis, these tumors are not only more likely to invade the myometrium but are significantly more prone to achieve deep invasion into the outer half.
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PMID:Adenomyosis involved by endometrial adenocarcinoma is a significant risk factor for deep myometrial invasion. 1763 Jan 8

Ureteral endometriosis is a rare yet important entity that can lead to renal failure due to silent obstruction of the ureter. Awareness of clinical and morphologic features can help in early detection and treatment. We analyzed the clinical, pathologic, and immunohistochemical findings of 7 cases of ureteral endometriosis. Mean age of patients was 51 years. All patients presented with hydroureter, accompanied in the most cases by hydronephrosis. Superimposed pyelonephritis was experienced by 2 of 7 patients. Most patients (4 of 7) had previously undergone total abdominal hysterectomy with bilateral salpingo-oophorectomy. In 6 of 7 cases, endometriosis involved the left ureter. The distal one third of the ureter was involved in 6 cases, whereas the middle third was involved in 1 case. In 4 cases, endometriosis was located extrinsic to the ureter, whereas in 3 cases, the ureter showed intrinsic involvement by endometriosis. One case showed simple endometrial hyperplasia. Surgical management included nephrectomy in 2 cases, distal ureterectomy with reimplantation in 3 cases, ureteral stent placement followed by ureteroureterostomy in 1 case, and relief of ureteral obstruction by resection of pelvic endometrioma in 1 case. Immunostains for cytokeratin-7 (CK7) and progesterone receptor (PR) were positive in all of the cases, whereas immunostains for estrogen receptor (ER) were positive in 83% of cases and immunostains for CK20 were negative in all cases. CA125 immunostains were positive in 67% of cases. The stromal cells were positive for CD10, ER, and PR immunostaining. Our findings suggest that the diagnosis of ureteral endometriosis is preceded in most cases by hysterectomy and bilateral salpingo-oophorectomy, possibly because of prior symptoms related to adenomyosis or pelvic endometriosis and that ureteral endometriosis has a strong predilection for involvement of the lower third of the left ureter. Ureteral endometriosis should be included in the differential diagnosis of obstructive ureteral lesions in women, particularly those involving the lower third of the left ureter, even in postmenopausal patients. Immunostains for ER, PR, CK7, CA125, and CD10 can be helpful in challenging cases.
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PMID:Ureteral endometriosis: clinicopathological and immunohistochemical study of 7 cases. 1853 72

The major differential diagnostic problem presented by atypical polypoid adenomyofibroma (atypical polypoid adenomyoma) (APA), which usually affects young women, is the exclusion of well-differentiated endometrial carcinoma invading the myometrium. This distinction, however, is of great clinical importance from the standpoint of treatment because reproductive conservation is feasible for patients with APA. Recently, CD10, known to be a marker of endometrial stromal cells, was reported to be also expressed in cells immediately surrounding the neoplastic glands invading the myometrium [Am J Surg Pathol 27 (2003) 786-789; Mod Pathol 16(1) (2003) 22-27]. However, CD10 expression in the myofibromatous component of APA has not been previously examined in the literature. We therefore decided to examine whether the CD10-immunostaining pattern in APA is different from that in myoinvasive carcinoma. Furthermore, we also attempted to obtain any histopathologic findings that may offer some insight regarding the histogenesis of APA. Seven cases of APA were immunostained for CD10 using curettage or polypectomy specimens, in addition to hysterectomy specimens in 1 case. Areas with more fibrotic rather than muscular stroma were focally observed in 4 cases. The pattern of staining was compared with hysterectomy specimens taken from 19 cases in which well- to moderately differentiated endometrioid adenocarcinoma had deeply invaded the myometrium (outer two thirds of the myometrium) but was not associated with adenomyosis. In 6 of 7 cases of APA, CD10 was never expressed in the myofibromatous stromal components. In 1 case of APA, the fascicles of fibrotic and muscular mesenchymal cells in the interglandular areas were focally and weakly positive for CD10. All 19 myoinvasive carcinomas expressed CD10 to some extent in cells immediately surrounding the neoplastic myoinvasive glands (fringe-like staining pattern). The proportion of the myoinvasive nests immediately surrounded by CD10-positive mesenchymal cells was as follows: mean, 74%; median, 80%; minimum, 5%; maximum, 100%. The fringe-like CD10-staining pattern was not observed in APA. Furthermore, we identified a gradual transformation from preexisting endometrial stromal cells (CD10 positive) into the typical myofibromatous stromal component (CD10 negative) of APA in 1 case. In conclusion, this study demonstrated differences in the CD10 immunoreactivity or immunostaining pattern between the stromal components of APA and myoinvasive endometrial carcinoma. This difference should lead to a more accurate diagnosis of APA (pseudo-myoinvasive lesion). Furthermore, the histogenesis of APA may perhaps be explained by "myofibromatous metaplasia" of the endometrial stromal cells.
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PMID:CD10 immunostaining distinguishes atypical polypoid adenomyofibroma (atypical polypoid adenomyoma) from endometrial carcinoma invading the myometrium. 1861 43


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